Regulation of cyclin D1 gene expression

2010 ◽  
Vol 38 (1) ◽  
pp. 217-222 ◽  
Author(s):  
Ini-Isabée Witzel ◽  
Li Fang Koh ◽  
Neil D. Perkins

Cyclin D1 is a key regulator of cell proliferation and its expression is subject to both transcriptional and post-transcriptional regulation. In different cellular contexts, different pathways assume a dominant role in regulating its expression, whereas their disregulation can contribute to overexpression of cyclin D1 in tumorigenesis. Here, we discuss the ability of the NF-κB (nuclear factor κB)/IKK [IκB (inhibitor of NF-κB) kinase] pathways to regulate cyclin D1 gene transcription and also consider the newly discovered role of the SNARP (SNIP1/SkIP-associated RNA processing) complex as a co-transcriptional regulator of cyclin D1 RNA stability.

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 757-760 ◽  
Author(s):  
Ronald A. Butow ◽  
Hong Zhu ◽  
Philip Perlman ◽  
Heather Conrad-Webb

All mRNAs on the yeast mitochondrial genome terminate at a conserved dodecamer sequence 5′-AAUAAUAUUCUU-3′. We have characterized two mutants with altered dodecamers. One contains a deletion of the dodecamer at the end of the var1 gene, and the other contains two adjacent transversions in the dodecamer at the end of the reading frame of fit1, a gene within the ω+ allele of the 21S rRNA gene. In each mutant, expression of the respective gene is blocked completely. A dominant nuclear suppressor, SUV3-1, was isolated that suppresses the var1 deletion but is without effect on the fit1 dodecamer mutations. Unexpectedly, however, we found that SUV3-1 blocks expression of the wild-type fit1 allele by blocking processing at its dodecamer. SUV3-1 has pleiotropic effects on mitochondrial gene expression, affecting RNA processing, RNA stability, and translation. Our results suggest that RNA metabolism and translation may be part of a multicomponent complex within mitochondria.Key words: mitochondria, yeast, mRNA, RNA processing, 3′ dodecamer.


2004 ◽  
Vol 279 (30) ◽  
pp. 31304-31311 ◽  
Author(s):  
Lawrence M. Pfeffer ◽  
Jong-Gwan Kim ◽  
Susan R. Pfeffer ◽  
Dennis J. Carrigan ◽  
Darren P. Baker ◽  
...  

Blood ◽  
2008 ◽  
Vol 112 (4) ◽  
pp. 1453-1460 ◽  
Author(s):  
Marcos Luengo-Blanco ◽  
Carolina Prando ◽  
Jacinta Bustamante ◽  
Walmir Cutrim Aragão-Filho ◽  
Paulo Vitor Soeiro Pereira ◽  
...  

AbstractThis work investigated the functional role of nuclear factor–κB (NF-κB) in respiratory burst activity and in expression of the human phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase genes CYBB, CYBA, NCF1, and NCF2. U937 cells with a stably transfected repressor of NF-κB (IκBα-S32A/S36A) demonstrated significantly lower superoxide release and lower CYBB and NCF1 gene expression compared with control U937 cells. We further tested Epstein-Barr virus (EBV)-transformed B cells from patients with anhidrotic ectodermal dysplasia with immunodeficiency (EDA-ID), an inherited disorder of NF-κB function. Superoxide release and CYBB gene expression by EDA-ID cells were significantly decreased compared with healthy cells and similar to cells from patients with X-linked chronic granulomatous disease (X910 CGD). NCF1 gene expression in EDA-ID S32I cells was decreased compared with healthy control cells and similar to that in autosomal recessive (A470) CGD cells. Gel shift assays demonstrated loss of recombinant human p50 binding to a NF-κB site 5′ to the CYBB gene in U937 cells treated with NF-κB inhibitors, repressor-transfected U937 cells, and EDA-ID patients' cells. Zymosan phagocytosis was not affected by transfection of U937 cells with the NF-κB repressor. These studies show that NF-κB is necessary for CYBB and NCF1 gene expression and activation of the phagocyte NADPH oxidase in this model system.


2010 ◽  
Vol 118 (12) ◽  
pp. 691-705 ◽  
Author(s):  
Stuart M. Robinson ◽  
Derek A. Mann

NF-κB (nuclear factor κB) is a heterodimeric transcription factor that is constitutively expressed in all cell types and has a central role as a transcriptional regulator in response to cellular stress. In the present review, we discuss the role of NF-κB signalling in the maintenance of liver homoeostasis as well as in the pathogenesis of a wide variety of conditions affecting the liver, including viral hepatitis, steatohepatitis, cirrhosis and hepatocellular carcinoma. Much of the current knowledge of NF-κB signalling in the liver relates to the canonical pathway, the IKK [IκB (inhibitor of κB) kinase] complex and the RelA subunit. We explore the weaknesses of the experimental approaches to date and suggest that further work is needed to investigate in detail the discreet functions of each of the Rel subunits in liver physiology and disease.


1999 ◽  
Vol 67 (8) ◽  
pp. 3872-3878 ◽  
Author(s):  
Naoki Mori ◽  
Kazunori Oishi ◽  
Borann Sar ◽  
Naofumi Mukaida ◽  
Tsuyoshi Nagatake ◽  
...  

ABSTRACT Persistent infection with Pseudomonas aeruginosaincreases interleukin-8 (IL-8) levels and causes dense neutrophil infiltrations in the airways of patients with chronic airway diseases. Recently, we have reported that nitrite reductase from P. aeruginosa induces the production of IL-8 in respiratory cells, including bronchial epithelial cells. To determine the molecular mechanism(s) of nitrite reductase-induced IL-8 expression in respiratory cells, A549 epithelial cells were transfected with plasmids containing serial deletions of the 5′-flanking region of the IL-8 gene and then exposed to nitrite reductase. Nitrite reductase significantly enhanced IL-8 gene promoter-driven reporter activity. This increased IL-8 gene expression was inhibited by mutating the nuclear factor-κB (NF-κB) binding element. Nitrite reductase enhanced nuclear localization of the NF-κB binding complex. Furthermore, nitrite reductase induced the degradation of IκBα, the major cytoplasmic inhibitor of NF-κB, and the expression of IκBα mRNA. These data support the critical role of the activation of NF-κB in nitrite reductase-induced IL-8 gene expression in airway epithelium.


2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Amandah Necker‐Brown ◽  
Andrew Thorne ◽  
Akanksha Bansal ◽  
Mahmoud Mostafa ◽  
Anthony Gerber ◽  
...  

2004 ◽  
Vol 279 (41) ◽  
pp. 42774-42786 ◽  
Author(s):  
Hidemitsu Nakajima ◽  
Hiroshi Nagaso ◽  
Nobukazu Kakui ◽  
Midori Ishikawa ◽  
Toyokazu Hiranuma ◽  
...  

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